S1 - ANSWER -Closing of mitral and tricuspid valve
- Beginning of systole
S2 - ANSWER - Closure of the aortic and pulmonic valve
- End of systole
Valvular stenosis - ANSWER the valve orifice is constricted and narrowed, impeding the forward flow of
blood and increasing the workload of the cardiac chamber proximal to the diseased valve.
Intraventricular or atrial pressure increases in the chamber to overcome resistance to flow through the
valve. Increased pressure causes the myocardium to work harder, causing myocardial hypertrophy.
Aortic stenosis - ANSWER - LV hypertrophy
- L heart failure
- Pulmonary edema
- Exertional dyspnea
-Syncope
, -Angina pectoris
- Systolic murmur
Mitral Stenosis - ANSWER - LA hypertrophy
-R ventricular failure
- Pulmonary edema
- Orthopnea
- Respiratory infections
- PH
-Edema
-Atypical chest pain
- Diastolic murmur
Stroke volume - ANSWER The volume of blood ejected per bear during systole
calcium binding and troponin - ANSWER In resting muscle the myosin-binding sites are covered by
troponin and tropomyosin. The calcium ions released into the sarcoplasm as a result of the action
potential bind to the troponin. This binding causes the tropomyosin and troponin to move out of the way
of the myosin-binding sites, leaving the myosin heads free to bind to the actin microfilament.
Macrophages - ANSWER -Phagocytic cells
-Involved in the activation of the adaptive immune system
-The primary cells that infiltrate tissue in wounds, remove cells and debris, promote angiogenesis, and
produce cytokines and growth factors that suppress further inflammation and initiate healing by
promoting epithelial cell division, activating fibroblasts and promote synthesis of extracellular matrix and
collagen.
- May appear at inflammatory site at 24 hours (but usually not until 3-7 days later)
- Survive and dive in the acidic inflammatory site
Perfusion - ANSWER Blood circulating past the alveloi
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